Acute promyelocytic leukaemia (APL) is an M3 subtype of acute myeloid leukaemia (AML). This classification is based on the morphology of promyelocytic cell. The clinical characteristics of APL can be recognized by haemorrhagic episodes, a differentiation block at the promyelocytic stage, and sensitivity to the differentiation response to all-trans-retinoic acid (ATRA). Cytogenetically, APL is characterized by a balanced reciprocal translocation between chromosomes 15 and 17, which results in the production of PML/RARα fusion protein. Recent studies reported that microRNAs (miRNAs) have also been proposed to contribute to the pathogenesis of APL. miRNAs have been associated with the pathogenesis of cancer and their involvement as oncogenic and tumour suppressor activities have been identified. They are involved in various biological processes including the cell proliferation, differentiation, growth and development, metabolism, apoptosis, and haematopoiesis. The new discovery of miRNAs as possible therapeutic markers will provide new insight for the diagnosis and therapeutic entries for the treatment of APL. This review highlights the potential of miRNAs as biomarkers in APL. 1. Introduction Acute promyelocytic leukaemia (APL) is identified as the M3 subtype of acute myeloid leukaemia (AML) by the French-American-British (FAB) classification. This classification is based on the percentage of maturing cells beyond the myeloblast stage. Bone marrow shows hypercellular promyelocytes and the most striking feature of these cells is the cytoplasmic hypergranularity. Multiple Auer rods are also observed in a few early cells in APL. According to WHO 2008 classification, APL is characterized by a reciprocal translocation between chromosomes 15 and 17, which results in the fusion between the promyelocytic leukaemia (PML) gene and retinoic acid receptor α (RARα) gene [1]. A schematic representation of the chromosomes and genes involved in t(15;17) is shown in Figure 1. Figure 1: Chromosomal reciprocal translocation of the 15th and 17th chromosomes. The breakpoints on chromosome 17 are consistently located within the second intron of the RARα gene, but, on chromosome 15, there are different breakpoint cluster regions, namely bcr1, bcr2, and bcr3 located in intron 6, exon 6, and intron 3, respectively, of the PML gene [2, 3]. The location of bcr1, bcr2, and bcr3 produces fusion transcripts of varying lengths referred to as the long, variant, and short forms, respectively [3]. This translocation can be detected by karyotyping or fluorescence in situ hybridization
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